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Jerry Silver, PhD
Professor
Department of Neurosciences
School of Medicine
Case Western Reserve University
Jerry Silver received a PhD from Case Western Reserve University in 1974, the university to which he returned after post-doctoral work at Harvard including the Neuropathology Department in Harvard Medical School, and the Department of Neurosciences at The Children's Hospital. Currently he is professor of Neuroscience at his alma mater, and adjunct professor in the Department of Neurosurgery at the nearby Cleveland Clinic Foundation. Dr. Silver has additionally served in the National Institutes of Health since 1982. He also received the 2003 Ameritec Prize and the Christopher Reeve-Joan Irvine Medal for his accomplishments in his work in paralysis and spinal cord injury. A prolific writer, Dr. Silver reviews articles for over 35 journals and also reviews grants from 18 both national and international groups. He has also taken part in authoring over 150 publications.

Over the past several years, Dr. Silver has concentrated his labs efforts learning whether molecules that glia produce to generate normal axon boundaries in the embryo are re-expressed by reactive glia in the scar that develops after injury. One of the most interesting families of extracellular matrix molecules, the proteoglycans, were first discovered by his lab to be major players in creating developmental as well as regenerative glial boundaries. He developed in vitro assays using gradients of proteoglycans that, like the in vivo glial scar, create dystrophic endings on regenerating adult axons. This breakthrough enabled him, for the first time, to begin to dissect the molecular and cellular machinery of this unusual axonal ending and learn why axons in a dystrophic state undergo long distance retraction from the lesion epicenter, how they interact with other types of cells, such as stem cells, inflammatory cells or CNS macroglia and how axons in the dystrophic state can be re-energized into a growth state. His ultimate goal is to develop strategies to overcome inhibitory molecules and axonal dieback after injury in order to promote functional regeneration. An exciting development is his recent demonstration that combining (1) a long segment of autologous peripheral nerve as a “bridge” to bypass a hemisection lesion of the adult rat spinal cord with (2) inhibitory matrix modification via chondroitinase at the PNS/CNS interface allows regenerating axons to exit the bridge, form functional synapses, and restore useful movement to the once paralyzed limb or diaphragm. This new strategy shows clearly, for the first time, that robust long distance regeneration, with appropriate re-formation of functional connections, can be achieved in the adult after spinal cord injury.